MANABU SASADA

Last Updated :2024/07/03

Affiliations, Positions
Hiroshima University Hospital(Clinical Research Center in Hiroshima), Associate Professor (Special Recognition)
E-mail
msasadahiroshima-u.ac.jp

Basic Information

Major Professional Backgrounds

  • 2020/04/01, 2020/06/30, Center For Integrated Medical Research, Hiroshima University Hospital, Assistant Professor
  • 2020/07/01, 2021/03/31, Clinical Research Center in Hiroshima, Hiroshima University Hospital, Assistant Professor
  • 2021/04/01, 2023/03/31, Ministory of Health, Labour and Welfare Goverment of Japan, Office of Medical Devices Policy, Health Policy Bureau, Officer
  • 2023/04/01, 2024/03/31, Ministry of Health, Labour and Welfare Goverment of Japan, Office of Medical Devices Policy, Policy Planning Division for Pharmaceutical Indusry Promotion and Medical Information Management, Health Policy Breau, Unit Chief
  • 2024/04/01, Clinical Research Center in Hiroshima, Hiroshima University Hospital, Assistant Professor

Research Fields

  • Biological Sciences;Oncology;Tumor therapeutics
  • Medicine,dentistry, and pharmacy;Basic medicine;Pathological medical chemistry
  • Medicine,dentistry, and pharmacy;Pharmacy;Biological pharmacy
  • Medicine,dentistry, and pharmacy;Society medicine;Medical and hospital management

Research Keywords

  • Cancer; neuroblastoma, glioma/glioblastoma, c-Myc, N-Myc, MYCN
  • Cell Adhesion; integrin, tenascin-C, fibronectin, extracellular matrix, senescence
  • Support for development of medical devices, regenerative cell therapy products and in vitro diagnostic products

Affiliated Academic Societies

  • The Pharmaceutical Society of Japan
  • The Japanese Association for Molecular Target Therapy of Cancer

Research Activities

Academic Papers

  1. Induction of cellular senescence in fibroblasts through beta1-integrin activation by tenascin-C-derived peptide and its protumor effect, American Journal of Cancer Research, 11(9), 4364-4379, 20211028
  2. The Promoting Effect of the Extracellular Matrix Peptide TNIIIA2 Derived from Tenascin-C in Colon Cancer Cell Infiltration, International Journal of Molecular Sciences, 20170117
  3. Combining peptide TNIIIA2 with all- trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells, American Journal of Cancer Research, 20190201
  4. Peptide TNIIIA2 Derived from Tenascin-C Contributes to Malignant Progression in Colitis-Associated Colorectal Cancer via beta1-Integrin Activation in Fibroblasts, International Journal of Molecular Sciences, 20190605
  5. Autocrine Production of PDGF Stimulated by the Tenascin-C-Derived Peptide TNIIIA2 Induces Hyper-Proliferation in Glioblastoma Cells, International Journal of Molecular Sciences, 20190628
  6. ★, Inactivation of beta1 integrin induces proteasomal degradation of Myc oncoproteins, Oncotarget, 20190813
  7. ★, Aggressive Progression in Glioblastoma Cells through Potentiated Activation of Integrin alpha5beta1 by the Tenascin-C-Derived Peptide TNIIIA2, Molecular Cancer Therapeutics, 20190918
  8. TAp63 represses transcription of MYCN/NCYM gene and its high levels of expression are associated with favorable outcome in neuroblastoma, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 518(2), 311-318, 2019
  9. Acyclic Retinoid Combined With Tenascin-C-derived Peptide Reduces the Malignant Phenotype of Neuroblastoma Cells Through N-Myc Degradation, Anticancer Research, 2019
  10. A novel method to purify neutrophils enables functional analysis of zebrafish hematopoiesis., Genes to cells : devoted to molecular & cellular mechanisms, 25(12), 2020
  11. Erratum: Combining peptide TNIIIA2 with all-trans retinoic acid accelerates N-Myc protein degradation and neuronal differentiation in MYCN-amplified neuroblastoma cells., American journal of cancer research, 10(1), 2020
  12. Involvement of Integrin-Activating Peptides Derived from Tenascin-C in Cancer Aggression and New Anticancer Strategy Using the Fibronectin-Derived Integrin-Inactivating Peptide., Molecules (Basel, Switzerland), 25(14), 2020
  13. Exposure of the cryptic de-adhesive site FNIII14 in fibronectin molecule and its binding to membrane-type eEF1A induce migration and invasion of cancer cells via β1-integrin inactivation., American journal of cancer research, 10(11), 2020
  14. Anoikis resistance conferred by tenascin-C-derived peptide TNIIIA2 and its disruption by integrin inactivation, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 536, 14-19, 20210115

Invited Lecture, Oral Presentation, Poster Presentation

  1. Combination of all-trans retinoic acid with tenascin-C derived peptide enhances neural differentiation of MYCN-amplified neuroblastoma cells, Manabu Sasada, Kazuki Otsuka, Yoichiro Isohama and Fumio Fukai, Yusuke Suenaga, Sana Yokoi, World Congress on Cancer Science and Therapy, 2019/07/15, Without Invitation, English, Henry Bruce, Rome, Italy, Neuroblastoma is one of the common pediatric tumors. Among the neuroblastoma patients, high-risk group is characterized by amplification of the MYCN gene, which codes N-Myc protein. Excessively expressed N-Myc protein inhibits neuronal differentiation during normal development, which is a central aspect of neuroblastoma genesis. Despite mass-chemotherapy, the survival rate for high-risk neuroblastoma remains extremely low. Besides this low treatment efficacy, mass-chemotherapy has additional severe side effects, so-called “late effects”, that occur many years after chemotherapy has ended. To solve this problem, differentiation therapy using retinoic acid and its derivatives has been expected as a mild chemotherapy with low risk of the late effects. However, the clinical outcome of differentiation therapy using retinoids including all-trans retinoic acid (ATRA) and its derivatives has not been sufficient due to the differentiation inhibition by over-expressed N-Myc protein. In the present study, we succeeded in synergistically accelerating the ATRA-induced neural differentiation of MYCN-amplified neuroblastoma cells by combining a peptide derived from tenascin-C, termed TNIIIA2, which has a potent ability to activate β1-integrins. Achievement of the high efficacy of neural differentiation was attributed to the induction of proteasome degradation of N-Myc protein by the combination of ATRA and TNIIIA2. Importantly, this enhanced differentiation was accompanied by a marked reduction of the malignant phenotype of neuroblastoma cells, and an in vivo experiment showed therapeutic potential of the combination therapy. These results provide a new insight into differentiation therapy for high-risk neuroblastoma based on N-Myc protein degradation.